{"id":523672,"date":"2022-05-26T10:50:58","date_gmt":"2022-05-26T14:50:58","guid":{"rendered":"https:\/\/www.rochester.edu\/newscenter\/?p=523672"},"modified":"2022-08-02T12:41:33","modified_gmt":"2022-08-02T16:41:33","slug":"the-secret-to-a-longer-lifespan-gene-regulation-holds-a-clue-523672","status":"publish","type":"post","link":"https:\/\/www.rochester.edu\/newscenter\/the-secret-to-a-longer-lifespan-gene-regulation-holds-a-clue-523672\/","title":{"rendered":"Gene regulation may hold clue to longer life"},"content":{"rendered":"

Rochester biologists who study the genetics of lifespan suggest novel targets to combat aging and age-related diseases.<\/h2>\n

Natural selection produces mammals that age at dramatically different rates. Take, for example, naked mole rats and mice. The former can live up to 41 years, nearly ten times as long as similar-size rodents such as mice.<\/p>\n

What accounts for longer lifespan? According to new research from Ä¢¹½´«Ã½<\/a> biologists, mechanisms controlling gene regulation are a key piece of the puzzle.<\/p>\n

In a paper published in Cell Metabolism<\/em><\/a>, the researchers, including Vera Gorbunova<\/a>, the Doris Johns Cherry professor of biology and medicine;\u00a0Andrei Seluanov<\/a>, professor of biology and medicine; and Jinlong Lu, a postdoctoral research associate in Gorbunova\u2019s lab and the first author of the paper, investigated genes connected to lifespan. Their research uncovered specific characteristics of these genes and revealed that two regulatory systems controlling gene regulation are critical to longevity. The findings help scientists better understand longevity and may provide new targets to combat aging and age-related diseases.<\/p>\n

Comparing gene regulation patterns<\/strong><\/h3>\n

The researchers compared the gene regulation patterns of 26 mammalian species with diverse maximum lifespans. The lifespans ranged from two years (shrews) to 41 years (naked mole rats). The researchers then identified thousands of genes related to a species\u2019 maximum lifespan. These genes were either positively or negatively correlated with longevity.<\/p>\n

They found that long-lived species tend to have low expression of genes involved in energy metabolism and inflammation. However, they have high expression of genes involved in DNA repair, RNA transport, and organization of cellular skeleton (or microtubules). Gorbunova and Seluanov showed in previous research that mammals with long lifespans have features such as more efficient DNA repair<\/a> and a weaker inflammatory response<\/a>.<\/p>\n

The opposite was true for short-lived species. Short-lived species tend to have high expression of genes involved in energy metabolism and inflammation. They have low expression of genes involved in DNA repair, RNA transport, and microtubule organization.<\/p>\n

Two pillars of longevity<\/strong><\/h3>\n

When the researchers analyzed the mechanisms that regulate these genes, they found two major systems at play. Circadian networks control the negative lifespan genes\u2014those involved in energy metabolism and inflammation. That is, the genes’ expression is limited to a particular time of day. This may help limit the overall expression of the genes in long-lived species.<\/p>\n

\"Infographic
In comparing the gene regulation patterns of 26 species with diverse lifespans, Rochester biologists Vera Gorbunova and Andrei Seluanov found that the characteristics of the different genes were controlled by circadian or pluripotency networks. (Ä¢¹½´«Ã½ illustration \/ Julia Joshpe)<\/figcaption><\/figure>\n

This means we can exercise at least some control over the negative lifespan genes.<\/p>\n

\u201cTo live longer, we have to maintain healthy sleep schedules and avoid exposure to light at night as it may increase the expression of the negative lifespan genes,\u201d Gorbunova says.<\/p>\n

On the other hand, the pluripotency network controls positive lifespan genes\u2014those involved in DNA repair, RNA transport, and microtubules. The pluripotency network helps in reprogramming somatic cells\u2014any cells that are not reproductive cells\u2014into embryonic cells. Embryonic cells can more readily rejuvenate and regenerate, by repackaging DNA that becomes disorganized as we age.<\/p>\n

\u201cWe discovered that evolution activated the pluripotency network to achieve longer lifespan,\u201d Gorbunova says.<\/p>\n

The pluripotency network and its relationship to positive lifespan genes is therefore \u201can important finding for understanding how longevity evolves,\u201d Seluanov says. \u201cFurthermore, it can pave the way for new antiaging interventions that activate the key positive lifespan genes. We would expect that successful antiaging interventions would include increasing the expression of the positive lifespan genes and decreasing the expression of negative lifespan genes.\u201d<\/p>\n

\n

Read more<\/strong><\/h3>\n
\n
\"logo\u2018Longevity gene\u2019 responsible for more efficient DNA repair<\/strong><\/a>
\nRochester researchers uncover more evidence that the key to the \u201cFountain of Youth\u201d may reside in a gene that is found to produce more potent proteins in species with longer lifespans.<\/span><\/div>\n
\"collageConnecting the dots between aging, Alzheimer\u2019s, and \u2018junk DNA\u2019<\/strong><\/a>
\nBiologists Vera Gorbunova and Andrei Seluanov join colleagues at Brown and NYU in the quest to find potential targets of treatments and therapeutics for neurodegenerative diseases.<\/span><\/div>\n
\"medallionWhy do naked mole rats live long, cancer-free lives?<\/strong><\/a>
\nRochester biologists were surprised to see that despite its remarkable longevity, the naked mole rat still has cells that undergo senescence, like the cells in much shorter-lived mice.<\/span><\/div>\n<\/div>\n

 <\/p>\n","protected":false},"excerpt":{"rendered":"

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